ArticleJournal of cellular physiology2013
Myocardin and microRNA-1 modulate bladder activity through connexin 43 expression during post-natal development.
Article in Journal of cellular physiology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 28 citations in OpenAlex.
- Mir-29 repression in bladder outlet obstruction contributes to matrix remodeling and altered stiffness.PloS one · 2013Trial
- The Role of microRNA in Overactive Bladder: Relationship and Clinical Correlation.Medicina (Kaunas, Lithuania) · 2025Article
- Mechanosensitivity Is a Characteristic Feature of Cultured Suburothelial Interstitial Cells of the Human Bladder.International journal of molecular sciences · 2020Article
- Connexins: Synthesis, Post-Translational Modifications, and Trafficking in Health and Disease.International journal of molecular sciences · 2018Review
- Botulinum toxin A-induced muscle paralysis stimulates Hdac4 and differential miRNA expression.PloS one · 2018Article
- Review
- Characterization of miRNA-regulated networks, hubs of signaling, and biomarkers in obstruction-induced bladder dysfunction.JCI insight · 2017Article
- Aberrant Expression of microRNA-9 Contributes to Development of Intracranial Aneurysm by Suppressing Proliferation and Reducing Contractility of Smooth Muscle Cells.Medical science monitor : international medical journal of experimental and clinical research · 2016Article
- Structural and functional changes in gap junctional intercellular communication in a rat model of overactive bladder syndrome induced by partial bladder outlet obstruction.Experimental and therapeutic medicine · 2016Article
- Regulation of connexin signaling by the epigenetic machinery.Biochimica et biophysica acta · 2016Review
- Regulation of Connexins Expression Levels by MicroRNAs, an Update.Frontiers in physiology · 2016Review
- MicroRNA MiR-199a-5p regulates smooth muscle cell proliferation and morphology by targeting WNT2 signaling pathway.The Journal of biological chemistry · 2015Article
- Myocardin in biology and disease.Journal of biomedical research · 2015Review
- Article
- Myocardin: new therapeutic agent in vascular disease?Arteriosclerosis, thrombosis, and vascular biology · 2013Article
Corrections and comments
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Authors and funding
7 authors at 3 institutions in 2 countries.
Funding
Abstract
Overactive bladder (OAB) is a pervasive clinical problem involving alterations in both neurogenic and myogenic activity. While there has been some progress in understanding neurogenic inputs to OAB, the mechanisms controlling myogenic bladder activity are unclear. We report the involvement of myocardin (MYOCD) and microRNA-1 (miR-1) in the regulation of connexin 43 (GJA1), a major gap junction in bladder smooth muscle, and the collective role of these molecules during post-natal bladder development. Wild-type (WT) mouse bladders showed normal development from early post-natal to adult including increases in bladder capacity and maintenance of normal sensitivity to cholinergic agents concurrent with down-regulation of MYOCD and several smooth muscle cell (SMC) contractile genes. Myocardin heterozygous-knockout mice exhibited reduced expression of Myocd mRNA and several SMC contractile genes concurrent with bladder SMC hypersensitivity that was mediated by gap junctions. In both cultured rat bladder SMC and in vivo bladders, MYOCD down-regulated GJA1 expression through miR-1 up-regulation. Interestingly, adult myocardin heterozygous-knockout mice showed normal increases in bladder and body weight but lower bladder capacity compared to WT mice. These results suggest that MYOCD down-regulates GJA1 expression via miR-1 up-regulation, thereby contributing to maintenance of normal sensitivity and development of bladder capacity.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.